De eerste studie (pdf link) laat het effect van DNP zien op het zaad van stieren. Daarbij is niet gekeken naar afwijken, maar naar de metabole effecten. Die zijn kort gezegd hetzelfde als in spiercellen. De tweede studie gaat wel in op afwijkingen in sperma van ratten door gebruik van DNP. De conclusie staat in het rood. De derde studie gaat in op de toxicologie van DNP in de testes. Het lijkt allemaal mee te vallen dus volgens mij geen reden voor paniek. Het lijkt me wel zaak dit in de openheid te gooien en als jullie de zwangerschap doorzetten in een vroeg stadium onderzoek te doen naar de ontwikkeling van de vrucht. Sterkte hiermee.
http://www.jbc.org/content/149/1/177.full.pdf
/LABORATORY ANIMALS: Developmental or Reproductive Toxicity/ ... /This/ study aimed at examining the in vivo effect of 2,4-dinitrophenol (DNP) on spermato/spermiogenesis in male rats, and at comparing it with those of 2-sec-butyl-4,6-dinitrophenol (DNBP)/, a structurally related testicular toxicant/. DNP was dissolved in corn oil and administered orally (5 mL/kg bw) to Jcl:SD rats, 12 males per group, once a day for 5 consecutive days at doses of 0, 7.5, 15, and 30 mg/kg. DNBP (7.5 mg/kg) was also given to a group of 12 rats in the same manner. Six animals each per group were necropsied at 3 (D3) and 14 (D14) days after the last dosing, and their testes, epididymides, seminal vesicles and prostates were weighed and examined histopathologically. Sperm numbers in the caput and cauda epididymides (right side) were counted, while cauda epididymal sperm was analyzed for morphological abnormality and motility. DNBP and 30 mg/kg of DNP significantly reduced body weights of animals during the 5-day administration period. Observations at D3 revealed that DNBP but not DNP suppressed the weights of seminal vesicle and prostate. A reduction in sperm motility, as well as an induction of sperm abnormalities (tailless), was also evident in DNBP-treated rats at D14. In the DNP treated animals, however, only a slight increase in the incidence of tailless sperm was found in the highest dose group at D14. These results demonstrate that DNP has a spermatotoxic effect, but it is much weaker than that of a structurally related compound, DNBP.
As the high dose level of DNP in the present study was nearly the maximum tolerated dose, a potential spermatotoxic risk of acute exposure to DNP is considered to be negligibly low.
[Takahashi K et al; J Toxicol Sci 28 (4): 336 (2003)] **PEER REVIEWED**
/LABORATORY ANIMALS: Developmental or Reproductive Toxicity/ The present review paper summarizes the data available in the literature concerning dinitrophenolic compounds and evaluates male reproductive toxicity in experimental animals. Gavage and feeding doses of 2-sec-butyl-4,6-dinitrophenol (dinoseb; CAS No. 88-85-7) manifested testicular toxicity, and 4,6-dinitro-o-cresol (DNOC; CAS No. 534-52-1) showed similar but weaker testicular toxicity in laboratory animals. Consecutive doses of dinoseb and DNOC by gavage seemed to induce spermatotoxicity by disturbing spermiogenesis or the maturation process of sperm in the epididymis, and the most probable target cells of spermatotoxicity were thought to be testicular spermatids in rats. Prolonged exposure to dinoseb and DNOC in the diet also induced testicular toxicity in rats. However, the feeding dose of dinoseb irreversibly affected the early stage of spermatogenesis and produced infertility in rats.
On the other hand, 2,4-dinitrophenol (DNP; CAS No. 51-28-5) did not show testicular toxicity in laboratory animals according to available literature. Further studies in laboratory animals with nitrophenolic compounds are required for clarification of their testicular toxicity and for risk assessment in humans.
[Matsumoto M et al; Reproductive Toxicol 26 (3-4): 185-90 (2008)] **PEER REVIEWED** PubMed Abstract